Isolation and Characterization of Micro-organisms with Industrial Importance From Sisal Bole Rots

Investigation of microorganisms naturally acclimatized to Agave hybrid H 11648 (sisal bole rot) was conducted, with the aim of isolating and characterizing Aspergillus niger strains for industrial use. Microorganism were identified morphologically and then confirmation made by polymerase chain reaction (PCR). Results showed the existence of four major groups, listed in order of abundances as follows; Aspergilli (36.0±0.8) %, Penicillin (28.0±0.1) %, Yeast (15.0±1.6) %and Fusarium (10.0±0.12) %. The main groups of Aspergilli strains were A. nidulans, A. tamari and A. niger in ratios (3:2:2), respectively. Several endo-spore forming non-enteric gram (-) rods and coccid bacteria identified by API20 NE identification systemincluded,Brevundimonas diminuta sp, Shewanella putrefaciens sp, Brevundimonas vesicularis sp and Pasteurella sp. Results showed that sisal bole rot stems hosts a high bio-diversity of microorganism species other than A. niger. Exploitation of the individual strains is recommended. This could eventually produce strains forprecursors of industrially and therapeutically metabolites

Identification and Characterization of Post-activated B Cells in Systemic Autoimmune Diseases

Autoimmune diseases (AID) such as systemic lupus erythematosus (SLE), primary Sjögren's syndrome (pSS), and rheumatoid arthritis (RA) are chronic inflammatory diseases in which abnormalities of B cell function play a central role. Although it is widely accepted that autoimmune B cells are hyperactive in vivo, a full understanding of their functional status in AID has not been delineated. Here, we present a detailed analysis of the functional capabilities of AID B cells and dissect the mechanisms underlying altered B cell function. Upon BCR activation, decreased spleen tyrosine kinase (Syk) and Bruton's tyrosine kinase (Btk) phosphorylation was noted in AID memory B cells combined with constitutive co-localization of CD22 and protein tyrosine phosphatase (PTP) non-receptor type 6 (SHP-1) along with hyporesponsiveness to TLR9 signaling, a Syk-dependent response. Similar BCR hyporesponsiveness was also noted specifically in SLE CD27- B cells together with increased PTP activities and increased transcripts for PTPN2, PTPN11, PTPN22, PTPRC, and PTPRO in SLE B cells. Additional studies revealed that repetitive BCR stimulation of normal B cells can induce BCR hyporesponsiveness and that tissue-resident memory B cells from AID patients also exhibited decreased responsiveness immediately ex vivo, suggesting that the hyporesponsive status can be acquired by repeated exposure to autoantigen(s) in vivo. Functional studies to overcome B cell hyporesponsiveness revealed that CD40 co-stimulation increased BCR signaling, induced proliferation, and downregulated PTP expression (PTPN2, PTPN22, and receptor-type PTPs). The data support the conclusion that hyporesponsiveness of AID and especially SLE B cells results from chronic in vivo stimulation through the BCR without T cell help mediated by CD40-CD154 interaction and is manifested by decreased phosphorylation of BCR-related proximal signaling molecules and increased PTPs. The hyporesponsiveness of AID B cells is similar to a form of functional anergy

A candidate gene study of the type I interferon pathway implicates IKBKE and IL8 as risk loci for SLE

Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease in which the type I interferon pathway has a crucial role. We have previously shown that three genes in this pathway, IRF5, TYK2 and STAT4, are strongly associated with risk for SLE. Here, we investigated 78 genes involved in the type I interferon pathway to identify additional SLE susceptibility loci. First, we genotyped 896 single-nucleotide polymorphisms in these 78 genes and 14 other candidate genes in 482 Swedish SLE patients and 536 controls. Genes with P<0.01 in the initial screen were then followed up in 344 additional Swedish patients and 1299 controls. SNPs in the IKBKE, TANK, STAT1, IL8 and TRAF6 genes gave nominal signals of association with SLE in this extended Swedish cohort. To replicate these findings we extracted data from a genomewide association study on SLE performed in a US cohort. Combined analysis of the Swedish and US data, comprising a total of 2136 cases and 9694 controls, implicates IKBKE and IL8 as SLE susceptibility loci (Pmeta=0.00010 and Pmeta=0.00040, respectively). STAT1 was also associated with SLE in this cohort (Pmeta=3.3 × 10−5), but this association signal appears to be dependent of that previously reported for the neighbouring STAT4 gene. Our study suggests additional genes from the type I interferon system in SLE, and highlights genes in this pathway for further functional analysis

Le territoire impossible des populations tribales du parc national Sanjay Gandhi (Mumbai, Inde)

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Techniques for quantifying the accuracy of gridded elevatian models and for mapping uncertainty in digital terrain analysis

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Low long-term erosion rates in high-energy moutain belts : insights from thermo- and biochronology in the Eastern Pyrenees.

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Response of upland catchments to environmental change in a temperate highland setting: initial results from the Velay, Massif Central, France

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